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Dendritic cell co-stimulatory and co-inhibitory markers in chronic HCV: an Egyptian study
Hanan Fouad1, Maissa Saeed El Raziky, Rasha Ahmed Abdel Aziz
1Hanan Fouad, Dina Sabry, Medical Biochemistry Department, Faculty of Medicine, Cairo University, 11562 Cairo, Egypt.
Insights
Hepatitis C virus (HCV) infection reduces dendritic cell (DC) co-stimulatory markers and increases co-inhibitory markers, with effects lessened in dialysis patients. These changes correlate with viral load and disease progression.
Area of Science:
- Immunology
- Hepatology
- Virology
Background:
- Dendritic cells (DCs) play a crucial role in immune responses.
- Hepatitis C virus (HCV) infection can dysregulate immune cell function.
- Uremia in hemodialysis patients may further impact immune status.
Purpose of the Study:
- To investigate co-stimulatory (CD83, CD86, CD40) and co-inhibitory (PD-L1) markers on DCs.
- To assess levels of Interleukin-10 (IL-10) and hyaluronic acid (HA).
- To correlate these markers with HCV disease activity, viral load, and fibrogenesis.
Main Methods:
- Real-time polymerase chain reaction (PCR) was used to assess DC markers in peripheral blood mononuclear cells.
- ELISA or similar assays were used for IL-10 and HA quantification.
- Study included 50 controls, 50 HCV patients, and 50 HCV patients undergoing hemodialysis.
Main Results:
- HCV infection significantly decreased co-stimulatory markers (CD83, CD86, CD40) and increased PD-L1 compared to controls.
- Co-stimulatory markers were higher, and PD-L1 lower in hemodialysis patients versus HCV patients.
- Elevated IL-10 and HA were observed in HCV groups; IL-10 higher, HA lower in hemodialysis patients. HA correlated with disease activity/fibrosis; IL-10 with fibrosis in HCV patients.
Conclusions:
- HCV infection impairs DC function by decreasing co-stimulatory markers and increasing co-inhibitory markers.
- Uremia exacerbates some of these immune dysregulations, though co-stimulatory markers are less affected.
- These DC marker alterations are linked to viral load and disease severity in HCV.
Aim:
To assess co-stimulatory and co-inhibitory markers of dendritic cells (DCs) in hepatitis C virus (HCV) infected subjects with and without uremia.
Methods:
Three subject groups were included in the study: group 1 involved 50 control subjects, group 2 involved 50 patients with chronic HCV infection and group 3 involved 50 HCV uremic subjects undergoing hemodialysis. CD83, CD86 and CD40 as co-stimulatory markers and PD-L1 as a co-inhibitory marker were assessed in peripheral blood mononuclear cells by real-time polymerase chain reaction. Interleukin-10 (IL-10) and hyaluronic acid (HA) levels were also assessed. All findings were correlated with disease activity, viral load and fibrogenesis.
Results:
There was a significant decrease in co-stimulatory markers; CD83, CD86 and CD40 in groups 2 and 3 vs the control group. Co-stimulatory markers were significantly higher in group 3 vs group 2. There was a significant elevation in PD-L1 in both HCV groups vs the control group. PD-L1 was significantly lower in group 3 vs group 2. There was a significant elevation in IL-10 and HA levels in groups 2 and 3, where IL-10 was higher in group 3 and HA was lower in group 3 vs group 2. HA level was significantly correlated with disease activity and fibrosis grade in group 2. IL-10 was significantly correlated with fibrosis grade in group 2. There were significant negative correlations between co-stimulatory markers and viral load in groups 2 and 3, except CD83 in dialysis patients. There was a significant positive correlation between PD-L1 and viral load in both HCV groups.
Conclusion:
A significant decrease in DC co-stimulatory markers and a significant increase in a DC co-inhibitory marker were observed in HCV subjects and to a lesser extent in dialysis patients.
